1.Seven strains of Trypanosoma cruzi, differing in host-background, geographic distribution, virulence, and history of laboratory propagation were found to be immunologically interrelated. After spontaneous or drug-induced recovery from infection with any one of these strains, mice were immune to repeated challenges with the lethal WBH-strain which killed all non-immunized controls within 13 days.
2.Mouse antisera to the seven T. cruzi strains agglutinated homologous and herologous cultures of the same species at dilutions up to 1:2400, but did not react with Leishmania donovani. Some of the antisera also contained lysins of low titer. Normal mouse sera had no agglutinating or lytic properties.
3.Passive immunization with mouse antisera of high agglutinating titer, or prolonged pre-treatment with formalinized crithidia, blood trypanosomes and lyophilized leishmania stages from infected spleen, did not protect mice significantly against WBH-strain.
4.The sera of four human Chagas' disease patients at dilutions up to 1:200 agglutinated living (but not killed) cultures of six T. cruzi strains. These cultures differed considerably in their response to the natural agglutinins in normal human sera. The “smooth” Culbertson-strain was least reactive with normal sera, hence most valuable as a diagnostic test-antigen.
5.A simple, rapid slide-agglutination routine for the diagnosis of Chagas' disease by means of Culbertson-strain T. cruzi is described.
6.Inter-strain immunity, the nature of the protective mechanism and the present status of clinical diagnosis of Chagas' disease are discussed.
Institute for Cancer Research, and Lankenau Hospital Research Institute, Philadelphia.